EXAM 2A TEST REVIEW

I. HbA1c + percentages
a. ***HEMOGLOBIN A1c  glycocyclated or glycated hemoglobin
b. 3-month average of blood glucose
c. PERCENTAGES:
i. Type 2 diabetes: ≥ 6.5%
1. Can reach 12-13% (VERY HIGH)
ii. Pre-diabetes: ≥ 5.6% but less than 6.5%
iii. Normal: < 5.6%
II. Basic understanding of pathway of DNA
a. DNA contains the info needed to produce proteins
b. Transcription (copying a segment of DNA) results in mRNA
i. mRNA  copy of the info in DNA needed to make a protein
c. mRNA leaves the nucleus and goes to a ribosome (“protein factory”)
d. amino acids (building blocks of protein) are carried to the ribosome by tRNAs containing the
code that matches that on the mRNA
e. During TRANSLATION, the info contained in mRNA is used to determine the number, types, and
arrangements of amino acids in the protein
III. Lipid levels
a. Insulin resistance  hyperinsulinemia  increased TGs  TGs are incorporated into VLDLC
and released into blood  increase LDLC and decrease HDLC
b. LOW HDLC
i. Men < 40 mg/dl
ii. Women < 50 mg/dl
IV. Most rapid replenishment for the body
a. High glycemic index, glucose, and CHO
V. Essential vs. non-essential amino acids
a. ESSENTIAL AMINO ACIDS (9)  can’t be made in the body; have to get from food
i. Histidine
ii. Isoleucine (BCAA)
iii. Leucine (BCAA)
iv. Lysine
v. Methionine
vi. Phenylalanine
vii. Threonine
viii. Tryptophan
ix. Valine (BCAA)
b. NONESSENTIAL AMINO ACIDS (11)  made in the body
i. Alanine
ii. Arginine
iii. Asparagine
iv. Aspartic acid
v. Cysteine
vi. Glutamic acid
vii. Glutamine
viii. Glycine
ix. Proline
x. Serine
xi. Tyrosine
VI. Digestibility of starches, relation to glycemic index and glycemic load
a. Starch = complex carb (polysaccharide) – SOLUBLE FIBER
i. Composed of many monosaccharide units – mainly glucose
ii. AMYLOPECTIN (80% of starch)
 1. Branched-chain starch with glucose linked by alpha bonds
2. Affects blood glucose more  HAS MORE SUGAR
iii. AMYLOSE (20% of starch)
1. Long chain of glucose linked by alpha bods
2. Found in veggies, beans, breads, pasta, rice
iv. Doesn’t affect blood cholesterol
v. Digested in the mouth (salivary amylase) into disaccharides
vi. Digested in the small intestine (pancreatic amylase)
b. GLYCEMIC INDEX – influenced by starch structure
i. Type of starch (amylopectin vs. amylose)
ii. Baking vs. red potatoes
iii. Different types of rice and pasta have different GI
VII. Sickle cell anemia
a. Caused by mutation/incorrect amino acid sequences
i. Error in the order of a primary structure of a protein
b. Crescent shaped RBCs
c. Change in hemoglobin structure leads to RBCs that can no longer carry oxygen efficiently
d. Symptoms: severe headaches, joint pain, convulsions, paralysis, abdominal pain
e. Treatment: blood transfusion, medication to increase RBC synthesis, bone marrow transplant
VIII. PKU - PHENYLKATONURIA
a. Genetic disorder – Conversion of phenylalanine to tyrosine cannot occur
i. Tyrosine becomes conditionally essential
b. Consequence: severe mental retardation
i. Screening for PKU in all newborns
c. Treatment:
i. Babies  special formula
ii. Children and adults  low protein diet and vitamin/mineral supplements
IX. Gout
a. Crystallization of uric acid within the joints  leads to painful inflammation
b. POSSIBLE CAUSE:
i. Purine is a colorless crystalline substance found in DNA and RNA
ii. Purine is converted to urate or uric acid
iii. Rich food sources of purine: meat and alcohol
c. REDUCE RISK OF GOUT:
i. Reduce intake of meat and alcohol
ii. Include low fat dairy in diet
1. Less purine
2. Contains casein and lactalbumin
X. Amino Acid Metabolism
a. Amino acids are taken to the liver through the hepatic portal vein
i. Combined into protein
ii. Converted into glucose or fat
iii. Used for energy needs
iv. Released back into the bloodstream
b. UREA that results from amino acid breakdown is a waste product made from ammonia (NH3)
and is excreted in urine
i. Nitrogen is released during amino acid breakdown
XI. Female vs. male protein intake
a. 1 g protein = 4 kcal
b. 2.2 g/kg for athletes
XII. GLYCEMIC INDEX
a. Blood glucose response to a given food compared to a standard (glucose, white bread)
 EQUATION; the incremental area under the blood glucose curve after the test meal is eaten DIVIDED
BY the corresponding area after the standard food is eaten MULTIPLIED BY 100
b. GLYCEMIC INDEX TEST
i. Subjects are given a test food and a standard food on separate days
ii. Each food contains 50 g of available CHO
iii. Change in blood glucose is measured for 2 hours
c. Low GI = below 55
d. Intermediate GI = between 55-70
e. High GI = above 70
f. INFLUENCED BY:
i. Fiber content – soluble fiber
ii. Starch structure
1. Type: amylopectin vs. amylose
2. Baking vs. red potatoes
3. Different types of race/pasta have different GI
iii. Food processing (grinding, rolling, pressing)
1. More processed  broken down faster by the body  higher GI
iv. Physical structure
v. Macronutrients – fat
vi. Acid
1. Lowers GI by slowing gastric emptying
vii. Sugar
XIII. GLYCEMIC LOAD
a. May be better to calculate glycemic load rather than glycemic index
i. TAKES INTO ACCOUNT THE SERVINGS NEEDED TO RAISE GLUCOSE
b. EQUATION: GI x grams of available CHO per serving MULTIPLIED BY 100
c. Low GL = below 15
d. Intermediate GL = between 15-20
e. High GL = above 20
XIV. Sugar alcohols
a. SORBITOL  derivative of glucose
b. XYLITOL  derivative of xylose
c. MANITOL  derivative of monosaccharide (fructose)
d. Found in diabetic candy and gum  good for diabetics
e. 1.5-3 kcal/gram
f. Doesn’t cause as rapid a rise in blood glucose as simple sugars
i. Doesn’t get broken down as quickly
g. Doesn’t cause cavities
h. Excessive consumption may cause diarrhea
i. Pulls water from the blood (plasma)
XV. ALTERNATIVE SWEETENERS
a. ASPARTAME
i. Added to food = NutraSweet
ii. Sold as powder = Equal
iii. Made up of phenylalanine and aspartic acid
iv. 4 kcal/gram but 180x sweeter than sucrose
1. Don’t need to use as much
v. Not linked to cancer
vi. Many complaints of headaches, dizziness, seizures, nausea, allergic reactions
vii. ACCEPTABLE DAILY INTAKE (FDA)
1. 50 mg/kg body weight
2. ~14 cans of diet soda or 80 packs of Equal per day in adults
viii. No tooth decay
 ix. Can’t be used in products that require cooking
1. There is no bulk to it
x. People with PKU (phenylketonuria) should NOT use aspartame
1. Lack the ability to break down phenylalanine in the product
2. Can lead to negative growing affects and decreased brain development (severe
mental retardation)
b. ACESULFAME-K
i. 200x sweeter than sucrose
ii. Provides no energy to the diet bc it isn’t broken down
iii. Can be used in baking (unlike aspartame)
1. Can provide a little more bulk
2. Still can’t break it down
c. SACCHARIN
i. Used widely in soft drinks and table sweeteners
ii. Alternative sweeteners  yields little to no energy
iii. First produced in 1879
iv. Linked with bladder cancer in animals
1. no longer listed as a potential cancer in humans
d. SUCRALOSE
i. 600x sweeter than sucrose
ii. 3 hydroxyl groups on sucrose are replaced by 3 chlorines
iii. Doesn’t break down under high heat and can be used for cooking/baking
XVI. Type 1 diabetes – Ketosis (DKA)
a. Not enough insulin  mobilization of body fat into liver cells and converted to ketone bodies 
ketone levels rise in blood  ketones excreted in urine and pull Na and K ions and water along
with them  ion imbalance (pulling in Na and K)
b. CONSEQUENCES: electrolyte imbalance, dehydration, coma, death
c. TREATMENT: insulin injections, fluids, Na and K (to normalize electrolyte balance)
XVII. GLP-1 satiety, ghrelin – hormones
XVIII. Whole wheat vs. whole grain
a. Whole grains  not completely broken down  more fiber and nutrients

I. DIABETES MELLITUS
a. Person WITH type 1 or 2 diabetes
i. Not “type 1 or 2 DIABETIC”
b. Hyperglycemia  high blood glucose
i. 100-125 mg/dl
1. Fasting blood glucose – 8 hours
2. “fasting diabetic”
ii. 126+  type 2 diabetes
c. Hypoglycemia  low blood glucose
i. < 50 mg/dl
d. Prevalence of diabetes
i. 4.9% in 1990 to 9/4% in 2015
ii. ½ to 1/3 don’t know they’re diabetic
iii. Increase due to: increasing obesity, high levels of physical inactivity, aging population

II. GESTATIONAL DIABETES

a. Pregnant women
b. TREATMENT
i. Control weight
ii. Treated with insulin and diet
iii. Mother and child at high risk for developing diabetes later
 c. WHY TREAT IT
i. Fetus size
ii. Delivery issues
iii. Increased BP during pregnancy (pre-eclampsia)  makes pregnancy high risk
d. Only way to get rid of gestational diabetes/pre-eclampsia  DELIVERY
e. SHOULDER DYSTOCIA
i. Obstructed labor  after delivery of the head, the anterior shoulder of the infant can’t
pass below (or requires significant manipulation to pass below) the pubic symphysis
ii. Diagnoses when the shoulders fail to delivery shortly after fetal head
iii. Damages brachial plexus  long term effects

TYPE 1 DIABETES – insulin deficient

I. Body doesn’t produce/secrete enough insulin
II. Beta cells (pancreas) aren’t working correctly
a. Pancreas has trouble producing/secreting insulin
b. Glucose accumulation
III. Often begins in late childhood (8-12 years)
a. Can’t diagnose at birth
IV. Very thirsty and frequent urination
a. Body is trying to filter out/dilute glucose
b. Increase plasma volume  increase BP
c. Glycated proteins bind and stiffen arteries  CVD
V. CAUSES:
a. Genetic link
b. Destruction of beta cells in the pancreas
VI. SYMPTOMS:
a. Excessive urination*
b. Excessive thirst*
c. Excessive hunger*
d. Unusual weight loss
i. Have to use alternative fuel source (glucose is staying in the blood and not getting into
the cell)  muscle (protein) breakdown for energy
e. Exhaustion
f. Blood glucose plummets
g. Glucagon is mis-secreted – needed to breakdown glucose
h. Irritability
i. Ketosis
i. Breakdown fat  end up with acidic ketone bodies
ii. Diabetic + ketoacidosis = diabetic ketoacidosis (DKA)
VII. TREATMENT:
a. Insulin therapy
i. Injections 2-6x a day; inhaled form, insulin pump
ii. HOW MUCH INSULIN?
1. Needs to be monitored
2. Need to know how sensitive you are to insulin
3. Exercise/athletes  very sensitive to insulin
a. HIGH INSULIN SENSITIVITY IS GOOD
4. Sedentary  less sensitive to insulin
b. Dietary measure
i. 3 regular meals + constant snacks (to maintain blood glucose)
ii. Carb counting
c. Exercise  to improve insulin sensitivity
i. Why prevent weight gain?  can adversely affect glycemia, lipids, BP
 d. Aspirin daily  works as preventative measure (esp. for cardiovascular health)
i. Prophylactic use
e. Medications to control lipids
VIII. Kidney can’t filter as well
a. Glomerulus isn’t working right  too much pressure/arterial damage  kidney disease
IX. Nerve damage

TYPE 2 DIABETES – insulin resistant

I. Insulin sensitivity/glucose intolerance
a. Body doesn’t react to insulin; doesn’t pull it out of the cell  cascade of reactions doesn’t happen
 no GLUT-4 translocation
II. Beta cell failure/exhaustion
a. Have to secrete so much insulin that they end up failing
b. Have to take 2-6 insulin shots/day
III. Sugar foot
a. Nerve damage
b. Capillary damage
c. Infection
d. amputation
IV. Eyes
a. Increased BP  increase vascular pressure  damage in the eye  blindness
V. 90% of all diabetes
VI. Usually begins after 40 years old
a. Takes a long time to become insulin INSENSITIVE (lose sensitivity)
VII. Starting at earlier age now
a. Children are now being diagnosed with T2D + needing to take insulin shots
VIII. CAUSE: INSULIN RESISTANCE
a. Abdominal obesity
i. Abdominal fat is very active; high turnover (store-burn-store-burn)
ii. No turnover  fat becomes toxic (TNF-alpha and IL-1  can damage other cells)
iii. Causes damage all over the body (esp. skeletal muscle)  T2D
iv. Especially bad  store fat in skeletal muscle/where it shouldn’t be (obese people store
fat here bc they have nowhere to put it)  pre-inflammatory markers (TNF-alpha, IL-1)
IX. RISK FACTORS
a. Abdominal obesity (in 80% of cases)
b. Sedentary lifestyle
c. Genetic predisposition
d. Ethnicity
i. African-Americans, Hispanics, Asians, American Indians
X. SCREENING
a. All adults over 45  every 3 years
b. TESTS
i. 8-HOUR FASTING BLOOD GLUCOSE
1. Diabetes: ≥ 126 mg/dL
2. Pre-diabetes: 100-125 mg/dL
a. High chance of becoming diabetic
3. Confirm by testing on different days
ii. 2-HOUR ORAL GLUCOSE TOLERANCE TEST (OGTT)
1. Description:
a. Overnight fast
b. Liquid containing 75 g glucose
c. Blood glucose measured for 2 hours
2. Diabetic:  200 mg/dL
 3. Pre-diabetic: 140-199 mg/dL
4. Normal: < 140 mg/dL
XI. Can “cure” diabetes
a. Susceptibility to regain type 2 diabetes is VERY HIGH
XII. SENSITIVITY
a. High sensitivity  0nly have to secrete a little bit of insulin in response to glucose in the blood
i. Better to have higher sensitivity
b. Low sensitivity  have to secrete more insulin/might have more insulin receptors
c. Exercise/maintaining healthy body weight improves insulin sensitivity
XIII. PREVENTION
a. Diet and exercise
XIV. MILD SYMPTOMS (esp. in early phase of disease)
a. FATIGUE
i. High blood glucose  glucose not getting to cells  cells have no energy  powerhouse
of the cell has to find alternative energy sources
b. NIGHTTIME URINATION
i. Drinking lots of water
ii. Body/kidneys still have to filter the glucose
XV. TREATMENT
a. Regular exercise  Achieve healthy weight
b. ORAL MEDICATIONS (ex: Metformin  doesn’t directly lower blood glucose; makes person
more insulin sensitive)
i. Decrease glucose production by liver
ii. Increases insulin production by pancreas
iii. Makes tissues more insulin sensitive
iv. Slows starch digestion and absorption of glucose in small intestine
c. Insulin injections sometime necessary
d. Aspirin (for CVD)
e. Lipid lowering medications